title: Cytokine pathways and interactions in alopecia areata.
abstract: Alopecia areata (AA) is an autoimmune disease resulting in the premature arrest of the follicular growth cycle clinically resulting in patchy, non-scarring hair loss. The presence of a dense follicular T cell infiltrate and variations in cytokines have led to the hypothesis that T cell activation and alterations in inflammatory mediators are crucial participants in the etiopathogenesis of the disease. Various studies suggest that the AA pathogenesis has a dominant TH1-mediated component, with potential involvement of the TH17 pathway. However, a fully integrated view of intersecting cytokine networks that support the autoimmune response in AA is lacking. A more precise understanding of cytokine pathways in disease is required to rationally explore cytokine targeted treatment strategies. Here, we comprehensively and critically review the current literature to provide a working framework regarding the complexity of T cell-cytokine interactions in AA, emphasizing the areas necessitating further research, particularly for the development of novel therapeutic options.
authors.affiliation: Department of Dermatology University at Buffalo and Roswell Park Cancer Institute Rm. 6082, Clinical and Translational Research Center 845 Ellicott St, Buffalo, NY 14203, USA.
authors.forename: Cerrene N
authors.initials: CN
authors.lastname: Giordano
authors.affiliation: Department of Dermatology University at Buffalo and Roswell Park Cancer Institute Rm. 6082, Clinical and Translational Research Center 845 Ellicott St, Buffalo, NY 14203, USA.
authors.forename: Animesh A
authors.initials: AA
authors.lastname: Sinha
mesh_terms: D000506:Alopecia Areata / Q000188:drug therapy / Q000276:immunology*; D000818:Animals; D016207:Cytokines / Q000037:antagonists & inhibitors / Q000502:physiology*; D005544:Forecasting; D006801:Humans; D015398:Signal Transduction; D013601:T-Lymphocytes / Q000502:physiology
chemical_list: D016207:Cytokines
keywords: T-lymphocytes; alopecia; autoantigens; autoimmunity; cytokines; proinflammatory